a1_The effect of different muscle shortening velocity was studied during cycling at a pedalling rate of 60 and 120 rev.min-1 on the [K+]v in 21 healthy young men (aged 22.5±2.2 years, body mass 72.7±6.4 kg, VO2max 3.720±0.426 l . min-1) performing an incremental exercise test until exhaustion. The power output increased by 30 W every 3 min, using an electrically controlled ergometer Ergoline 800S (see Zoladz et al. J. Physiol. 488: 211-217, 1995). The test was performed twice: once at a cycling frequency of 60 rev.min-1 (test A) and a few days later at frequency of 120 rev.min-1 (test B). At rest and at the end of each step (i.e. the last 15 s) antecubital venous blood samples for [K+]v were taken. Gas exchange variables were measured continuously (breath-by-breath) using Oxycon Champion Jaeger. The pre-exercise [K+]v in both tests was not significantly different amounting to 4.24±0.36 mmol.l-1 in test A, and 4.37±0.45 mmol.l-1 in test B. However, the [K+]v during cycling at 120 rev.min-1 was significantly higher (p<0.001, ANOVA for repeated measurements) at each power output when compared to cycling at 60 rev.min-1. The maximal power output reached 293±31 W in test A which was significantly higher (p<0.001) than in test B, which amounted to 223±40 W. The VO2max values in both tests reached 3.720±0.426 l.min-1 vs 3.777±0.514 l.min-1. These values were not significantly different. When the [K+]v was measured during incremental cycling exercise, a linear increase in [K+]v was observed in both tests. However, a significant (p<0.05) upward shift in the [K+]v and a % VO2max relationship was detected during cycling at 120 rev.min-1. The [K+]v measured at the VO2max level in tests A and B amounted to 6.00±0.47 mmol.l-1 vs 6.04±0.41 mmol.l-1, respectively., a2_This difference was not significant. It can thus be concluded that a) generation of the same external mechanical power output during cycling at a pedaling rate of 120 rev.min-1 causes significantly higher [K+]v changes than when cycling at 60 rev.min-1, b) the increase of venous plasma potassium concentration during dynamic incremental exercise is linearly related to the metabolic cost of work expressed by the percentage of VO2max (increase as reported previously by Vollestad et al. J. Physiol. Lond. 475: 359-368, 1994), c) there is a tendency towards upward shift in the [K+]v and % VO2max relation during cycling at 120 rev.min-1 when compared to cycling at 60 rev.min-1., J. A. Zoladz, K. Duda, J. Majerczak, P. Thor., and Obsahuje bibliografii
In the present study we aimed to evaluate whether oxidative stress and inflammation induced by strenuous exercise affect glycocalyx integrity and endothelial function. Twenty one young, untrained healthy men performed a maximal incremental cycling exercise - until exhaustion. Markers of glycocalyx shedding (syndecan-1, heparan sulfate and hyaluronic acid), endothelial status (nitric oxide and prostacyclin metabolites - nitrate, nitrite, 6-keto-prostaglandin F1α), oxidative stress (8-oxo-2’- deoxyguanosine) and antioxidant capacity (uric acid, nonenzymatic antioxidant capacity) as well as markers of inflammation (sVCAM-1 and sICAM-1) were analyzed in venous blood samples taken at rest and at the end of exercise. The applied strenuous exercise caused a 5-fold increase in plasma lactate and hypoxanthine concentrations (p<0.001), a fall in plasma uric acid concentration and non-enzymatic antioxidant capacity (p<10−4), accompanied by an increase (p=0.003) in sVCAM-1 concentration. Plasma 6-keto-prostaglandin F1α concentration increased (p=0.006) at exhaustion, while nitrate and nitrite concentrations were not affected. Surprisingly, no significant changes in serum syndecan-1 and heparan sulfate concentrations were observed. We have concluded, that a single bout of severe-intensity exercise is well accommodated by endothelium in young, healthy men as it neither results in evident glycocalyx disruption nor in the impairment of nitric oxide and prostacyclin production., J. Majerczak, K. Duda, S. Chlopicki, G. Bartosz, A. Zakrzewska, A. Balcerczyk, R. T. Smoleński, J. A. Zoladz., and Obsahuje bibliografii
In this study we have evaluated the effect of maximal incremental cycling exercise (IE) on the systemic release of prostacyclin (PGI2), assessed as plasma 6-keto-PGF1α concentration in young healthy men. Eleven physically active - untrained men (mean ± S.D.) aged 22.7 ± 2.1 years; body mass 76.3 ± 9.1 kg; BMI 23.30 ± 2.18 kg · m-2; maximal oxygen uptake (VO2max) 46.5 ± 3.9 ml · kg-1 · min-1, performed an IE test until exhaustion. Plasma concentrations of 6-keto-PGF1α, lactate, and cytokines were measured in venous blood samples taken prior to the exercise and at the exhaustion. The net exercise-induced increase in 6-keto-PGF1α concentration, expressed as the difference between the end-exercise minus pre-exercise concentration positively correlated with VO2max (r=0.78, p=0.004) as well as with the net VO2 increase at exhaustion (r=0.81, p=0.003), but not with other respiratory, cardiac, metabolic or inflammatory parameters of the exercise (minute ventilation, heart rate, plasma lactate, IL-6 or TNF-α concentrations). The exercise-induced increase in 6-keto-PGF1α concentration was significantly higher (p=0.008) in a group of subjects (n=5) with the highest VO2max when compared to the group of subjects with the lowest VO2max, in which no increase in 6-keto-PGF1α concentration was found. In conclusion, we demonstrated, to our knowledge for the first time, that exercise-induced release of PGI2 in young healthy men correlates with VO2max, suggesting that vascular capacity to release PGI2 in response to physical exercise represents an important factor characterizing exercise tolerance. Moreover, we postulate that the impairment of exercise-induced release of PGI2 leads to the increased cardiovascular hazard of vigorous exercise., J. A. Zoladz ... [et al.]., and Obsahuje seznam literatury
In this experiment we studied the effect of different pedalling rates during cycling at a constant power output (PO) 132±31 W (mean±S.D.), corresponding to 50 % V02 max, on the oxygen uptake and the magnitude of the slow component of V02 kinetics in humans. The PO corresponded to 50 % of V02 max, established during incremental cycling at a pedalling rate of 70 rev.min-1. Six healthy men aged 22.2 ±2.0 years with V02 max 3.89 ±0.92 l.min-1, performed on separate days constant PO cycling exercise lasting 6 min at pedalling rates 40, 60, 80, 100 and 120 rev.min-1, in random order. Antecubital blood samples for plasma lactate [La]pi and blood acid-base balance variables were taken at 1 min intervals. Oxygen uptake was determined breath-by-breath. The total net oxygen consumed throughout the 6 min cycling period at pedalling rates of 40, 60, 80, 100 and 120 rev.min-1 amounted to 7.727± 1.197, 7.705± 1.548, 8.679± 1.262, 9.945± 1.435 and 13.720± 1.862 1, respectively for each pedalling rate. The VO2 during the 6 min of cycling only rose slowly by increasing the pedalling rate in the range of 40-100 rev.min-1. This increase, was 0.142 1 per 20 rev.min-1 on the average. Plasma lactate concentration during the sixth minute of cycling changed little within this range of pedalling rates: the values were 1.83 ±0.70, 1.80 ± 0.48, 2.33 ±0.88 and 2.52 ±0.33 mmoLl-1. The values of [La]pi reached in the 6th minute of cycling were not significantly different from the pre-exercise levels. Blood pH was also not affected by the increase of pedalling rate in the range of 40-100 rev.min-1. However, an increase of pedalling rate from 100 to 120 rev.min-1 caused a sudden increase in the VO2 amounting to 0.747 1 per 20 rev.min-1, accompanied by a significant increase in [La]pj from 1.21 ±0.26 mmol.l-1 in pre-exercise conditions to 5.92±2.46 mmol.l-1 reached in the 6th minute of cycling (P<0.01). This was also accompanied by a significant drop of blood pH, from 7.355 ±0.039 in the pre-exercise period to 7.296 ± 0.060 in the 6th minute of cycling (P<0.01). The mechanical efficiency calculated on the basis of the net VO2 reached between the 4th and the 6th minute of cycling amounted to 26.6 ±2.7, 26.4±2.0, 23.4±3.4, 20.3 ±2.6 and 14.7±2.2 %, respectively for pedalling rates of 40, 60, 80,100 and 120 rev.min-1. No significant increase in the VO2 from the 3rd to the 6th min (representing the magnitude of the slow component of V02 kinetics) was observed at any of the pedalling rates (-0.022±0.056, -0.009±0.029, 0.012±0.073, 0.030±0.081 and 0.122±0.176 l.min-1 for pedalling rates of 40, 60, 80, 100 and 120 rev.min-1, respectively). Thus a significant increase in [La]pi and a decrease in blood pH do not play a major role in the mechanism(s) responsible for the slow component of VO2 kinetics in
humans.